Strain-dependent effects of developmental ethanol exposure in zebrafish

Loucks, Evyn J.; Carvan, Michael J.

doi:10.1016/j.ntt.2004.06.017

Cited by 122 publications

(75 citation statements)

References 51 publications

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“…Recently three laboratories independently documented measurable ethanol-induced phenotypic features in zebrafish that could be utilized further for analysis of ethanol-responsive genes (Bilotta et al, 2004;Carvan et al, 2004;Loucks and Carvan, 2004;Reimers et al, 2004a). As shown here and in previous studies, the Japanese medaka is an alternative non-mammalian model, in addition to zebrafish, to evaluate ethanol toxicity.…”

Section: Discussionmentioning

confidence: 62%

Japanese medaka (Oryzias latipes): developmental model for the study of alcohol teratology

Wang

Williams

Haasch

et al. 2006

Birth Defects Research Pt B

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BACKGROUND: Animal models are necessary to investigate the mechanism of alcohol-induced birth defects. We have used Japanese medaka (Oryzias latipes) as a non-mammalian model to elucidate the molecular mechanism(s) of ethanol teratogenesis. METHODS: Medaka eggs, within 1 hr post-fertilization (hpf) were exposed to waterborne ethanol (0-1000 mM) in hatching solution for 48 hr. Embryo development was observed daily until 10 days post-fertilization (dpf). The concentration of embryonic ethanol was determined enzymatically. Cartilage and bones were stained by Alcian blue and calcein, respectively and skeletal and cardiovascular defects were assessed microscopically. Genetic gender of the embryos was determined by PCR. Levels of two isoenzymes of alcohol dehydrogenase (Adh) mRNAs were determined by semi-quantitative and real-time RT-PCR. RESULTS: The concentration of ethanol required to cause 50% mortality (LC 50 ) in 10 dpf embryos was 568 mM, however, the embryo absorbed only 15-20% of the waterborne ethanol at all ethanol concentrations. The length of the lower jaw and calcification in tail fin cartilaginous structures were reduced by ethanol exposure. Active blood circulation was exhibited at 501 hpf in embryos treated with 0-100 mM ethanol; active circulation was delayed and blood clots developed in embryos treated with 200-400 mM ethanol. The deleterious effects of ethanol were not gender-specific. Moreover, ethanol treatment was unable to alter the constitutive expression of either Adh5 or Adh8 mRNA in the medaka embryo. CONCLUSIONS: Preliminary results suggested that embryogenesis in medaka was significantly affected by ethanol exposure. Phenotypic features normally associated with ethanol exposure were similar to that observed in mammalian models of fetal alcohol syndrome. The results further indicated that medaka embryogenesis might be used as an alternative non-mammalian model for investigating specific alterations in gene expression as a means to understand the molecular mechanism(s) of ethanol-induced birth defects.

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Section: Discussionmentioning

confidence: 62%

Japanese medaka (Oryzias latipes): developmental model for the study of alcohol teratology

Wang

Williams

Haasch

et al. 2006

Birth Defects Research Pt B

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“…For example, it has recently been shown that zebrafish strains exhibit different phenotypic effects when exposed to ethanol (34). Based on the phenotypes examined, individual strains exhibited differences in sensitivity to ethanol with regard to each pathway examined.…”

Section: Resultsmentioning

confidence: 99%

Extensive genetic diversity and substructuring among zebrafish strains revealed through copy number variant analysis

Brown

Dobrinski

Lee

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

102

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Copy number variants (CNVs) represent a substantial source of genomic variation in vertebrates and have been associated with numerous human diseases. Despite this, the extent of CNVs in the zebrafish, an important model for human disease, remains unknown. Using 80 zebrafish genomes, representing three commonly used laboratory strains and one native population, we constructed a genome-wide, high-resolution CNV map for the zebrafish comprising 6,080 CNV elements and encompassing 14.6% of the zebrafish reference genome. This amount of copy number variation is four times that previously observed in other vertebrates, including humans. Moreover, 69% of the CNV elements exhibited strain specificity, with the highest number observed for Tubingen. This variation likely arose, in part, from Tubingen's large founding size and composite population origin. Additional population genetic studies also provided important insight into the origins and substructure of these commonly used laboratory strains. This extensive variation among and within zebrafish strains may have functional effects that impact phenotype and, if not properly addressed, such extensive levels of germ-line variation and population substructure in this commonly used model organism can potentially confound studies intended for translation to human diseases.

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“…28,29,32 However, the developing embryo can show varying ethanol sensitivities based on genetic backgrounds (Ekkwill, AB, or Tu). 33 Interestingly, the tissues most affected by ethanol exposure varied among the different backgrounds with Tu having the lowest survival rate, but being the most resistant to craniofacial malformations. Work in different adult zebrafish backgrounds (wild-type AB, wild-type long fin, wild-type short fin, or Leopard danio) demonstrated that the backgrounds exhibited different sensitivities to ethanol, while tissue levels of ethanol were consistent across the backgrounds.…”

Section: Models Of Fasd: Return Of the Fishmentioning

confidence: 99%

“…83 Studies in mice, chick, and zebrafish show that different strains have different sensitivities to ethanol-induced defects. 33,34,[84][85][86] However, direct analysis of the genetic loci regulating sensitivity to ethanolinduced birth defects is still in its infancy. Only a handful of gene-ethanol interactions have been identified to date.…”

Section: Identifying Gene-ethanol Interactions: the Way Of The Fishmentioning

confidence: 99%

Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis

2016

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Fetal Alcohol Spectrum Disorders (FASD) describes a wide array of ethanol-induced developmental defects, including craniofacial dysmorphology and cognitive impairments. It affects *1 in 100 children born in the United States each year. Due to the pleiotropic effects of ethanol, animal models have proven critical in characterizing the mechanisms of ethanol teratogenesis. In this review, we focus on the utility of zebrafish in characterizing ethanolinduced developmental defects. A growing number of laboratories have focused on using zebrafish to examine ethanol-induced defects in craniofacial, cardiac, ocular, and neural development, as well as cognitive and behavioral impairments. Growing evidence supports that genetic predisposition plays a role in these ethanol-induced defects, yet little is understood about these gene-ethanol interactions. With a high degree of genetic amenability, zebrafish is at the forefront of identifying and characterizing the gene-ethanol interactions that underlie FASD.

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Strain-dependent effects of developmental ethanol exposure in zebrafish

Cited by 122 publications

References 51 publications

Japanese medaka (Oryzias latipes): developmental model for the study of alcohol teratology

Japanese medaka (Oryzias latipes): developmental model for the study of alcohol teratology

Extensive genetic diversity and substructuring among zebrafish strains revealed through copy number variant analysis

Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis

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